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2.4 Playing Dirty (1)

Genetic diversity allows us to have access to a repertoire of genetic tools that can help up function better in our environment. Diverse genetic stories give our microbial communities resilience to sudden or not so sudden environmental changes. Thus, with a diverse microbiome, we can encounter disruptions (and we do) that threaten the homeostasis of our health, but never actually cause it to shift—we stay healthy. Unfortunately, the Western diet seems to threaten that diversity. So rather than being islands of thriving life, the Western diet seems to lead to gut disorders like obesity, metabolic syndrome, and IBD. In ecosystem terms, we become like the Mississippi Delta, rife with blooms of organisms that choke out diversity. In talking about obesity, Peter Turnbaugh aptly describes this state:

This reduced diversity [in obese individuals] suggests an analogy: the obese gut microbiota is not like a rainforest or a reef, which are adapted to high energy flux and are highly diverse; rather, it may be more like a fertilizer run off where a reduced-diversity microbial community blooms with abnormal energy input[i].

Though our gut ecosystem has been recently implicated in many disorders ranging from gut disease and autoimmune disorders to mental states, the first real look at how our internal bionts influence our human system was done in obesity studies by the Gordon Group at Washington University of Medicine. They have done lots of research on feces and fat and have found that while all members of a mammalian species will share a core metabolism and phyla-level types of bacteria (so mice have a mouse core metabolism and phyla profile and humans have a core metabolism and phyla profile—but mice and human cores are not the same as each other, just as the human handprint and the mouse paw print differ) certain aspects of that core can be shifted, enhanced, or depleted. Such is the case in obese individuals.

According to the five-fingered hand model of our microbial make-up, the phyla Firmicutes and Bacteriodetes make up most of our microbiota followed by Actinobacteria, Proteobacteria, and Verricumicrobia/other microbes. Some research has linked the ratio of the size of the Bacteriodetes finger to the Firmicute finger to the lean or obese phenotype. In mouse studies, the relative abundance of Bacteriodetes fell by 50% in obese mice who lacked the gene to control their appetite and ate to excess[1], while the relative abundance of Firmicutes rose 50% compared to their lean mousey counterparts[ii]. Of interest was that the increase in Firmicutes was usually a bloom of one dominant genus that was very good at processing the excess food (read: fats, simple sugars, and refined carbohydrates) but was less adept at other important metabolic functions. In the face of an energy glut, the microbes that thrived got very good a processing energy into growth for themselves, at the expense of other metabolic and defensive functions. Therefore, as the ecosystem experienced inflation in nutrient availability, microbial functional diversity was lost as well as metabolic diversity. Further, these scientists found that obese mice shared more similar microbial metabolic abilities with other obese mice than those of their lean siblings.

[1] These genetically obese mice are called ob/ob mice and have a mutation in the gene that produces the hormone leptin. Leptin in both mice and humans controls appetite and, along with other hormones, signals when we have eaten enough. It tells us when we are sated and can stop eating. Mice (and people) who lack this key hormone cannot tell when they should stop eating and thus overeat, becoming obese. However, it is interesting that we can actually eat beyond these controls and do so regularly. This ability to disregard our bodies’ signals probably served an evolutionary advantage when times of gorging were few and far between.